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In this line of research, novel therapies aim to target apoptosis via mitochondria, using molecules that mimic BH3 proteins and disrupt the interactions of pro-apoptotic and anti-apoptotic proteins.

Therefore, the mechanisms by which mushroom extracts or isolated compounds induce mitochondrial-related apoptosis pathways are diverse and may be related with specific bioactive compounds. Modulation of pathways crucial for cell survival and alterations in lipid homeostasis seem to be related with the pro-apoptotic effects observed in HCC cell lines and in in-vivo xenograft models.

To sum up, mitochondria play a central role in the pathophysiology and progression of NAFLD as well as in the development of HCC, which can be a late-stage consequence of NASH. Hepatic mitochondria undergo bioenergetic remodelling to face the metabolic burden imposed by the increased FFAs load secondary to systemic IR. In turn, a decompensation of these processes may result in ROS formation and mitochondrial dysfunction, contributing to the development of NASH. Lastly, hepatic mitochondria also seem to be involved in anti-apoptotic oncogenic processes driving HCC. Targeting mitochondrial dysfunction is thus a promising approach for the treatment of the NAFLD continuum. The following section describes some of the in-vitro and in-vivo studies on the beneficial effects of mushroom-enriched diets or mushroom-derived compounds/extracts (Box 2) in preventing/reverting such liver damage.

Using this acoustic method, the presence of species, and a determination of ecological health, can be inferred simply by listening to the natural world without disturbing the environment or harming the plants and animals within it.

Publication: Jack A. Greenhalgh, et al., Diel variation in insect-dominated temperate pond soundscapes and guidelines for survey design, Freshwater Biology (2023). DOI: 10.1111/fwb.14092.

It is encouraging that heated insecticide killed highly resistant mosquitoes, says Hemingway, who directs the Infection Innovation Consortium, a public-private effort to find new ways to combat infectious diseases. But, she says, “this is not something we can take and use that tomorrow.”

“There are all kinds of social and cultural things that you could propose from a scientific perspective that wouldn’t be welcomed by a community of homeowners.”

Kahr and colleagues previously discovered that heating deltamethrin changed its crystal structure, which let it work faster

ompound called UM171,

specific polymer, improved the results by supporting long-term HSC expansion.

which might represent a novel non-toxic alternative to conventional cancer therapy available today.

These results clearly indicate that dandelion root extract can inhibit the ability of colorectal cancer cells to migrate and invade, and therefore metastasize to secondary locations.

morphological differences in tissue slices between the control untreated and the DRE treated group

aken together, these results established that systemic oral intake of the DRE was safe and its anti-cancer efficacy should be further investigated.

, but the DRE treatment efficiently suppressed the growth of both p53 WT and p53 mutant tumors in-vivo (Figure 4B – 4C)

with no difference between the control and DRE treated samples of NCM460

We observed a decrease in the viability of cells treated with α-amyrin, with 10 μM as the most effective concentration.

The results showed a progressive destabilization of the mitochondrial membrane following the DRE treatment, which was observed as early as 30 minutes post treatment (Figure ​6C). Pro-caspase-8 (green) was localized in the mitochondria (red) in control untreated cells; however, following the DRE treatment, activated caspase-8 was released from the mitochondria into cytoplasmic space, as indicated by the dispersed green fluorescence (Figure ​6C

suggesting that in HT-29 colorectal cancer cells the DRE-induced cell death was caspase-8 independent.

Others suggest that following activation, caspases re-localize to the mitochondria, where they interact with other pro-apoptotic proteins during the progression of apoptosis [15]. A third option, put forward by Qin and colleagues, suggests that inactive caspases are kept in the mitochondria, but following apoptotic stimuli and activation, they are released from the mitochondria into the cytoplasmic peri-nuclear space [

However, these results indicate that DRE and its anti-cancer components must be absorbed and circulated, in order to reach the site of the tumor (in order to inhibit tumor growth).

, we confirmed the vulnerability of cancer cell mitochondria by showing that the DRE treatment led to a decrease in the mitochondrial membrane potential and increase in ROS levels in the isolated mitochondria.

caspase-8 specific inhibitor, IETD-fmk, did not change the DRE response in these cells. This was in contrast to our previous study in leukemia and pancreatic cancer cells

he pro-apoptotic genes including Caspase-1, Interferon gamma and the TNF ligands and receptors, were up-regulated in HT-29 cells, prior to the apoptosis induction, while the same genes were down-regulated in NCM460 cells.

Previous findings show that taraxasterol has anti-inflammatory and chemopreventive activit

suggesting its importance in the anti-cancer activity of dandelion root extract, especially on the expression levels of COX-2. Additionally, we show that 10 μM lupeol is not very effective on its own

“If you can play everything backwards, then no energy has escaped during your computation,” says Demaine.